Further abstracts you may be interested in

Introduction: A general characteristic for NETs is their expression of certain proteins, such as chromogranin A (CgA), which is released from the dense core vesicles of NE cells, occasionally together with cell specific hormones, such as gastrin and serotonin. Plasma CgA seems to be closely related to tumor burden of intestinal carcinoid tumors in humans.

Introduction: Gastric endocrine tumors (GET) are increasingly recognized due to expanding indications of upper gastrointestinal endoscopy. Often silent and benign, GET may also be aggressive when sporadic and may sometimes mimic the course of gastric adenocarcinoma. Current incidence of GETs is estimated at around 8% of digestive endocrine tumors. Yearly age-adjusted incidence is around 0.2 per population of 100,000. Gastric carcinoids (ECLomas) develop from gastric enterochromaffin-like cells (ECL cells) in response to chronically elevated gastrin. Type 1 tumors (ECLomas in the course of atrophic gastritis) may occur in conditions of achlorhydria secondary to auto-immune atrophic fundic gastritis. It occurs mostly in women and they are non-functioning tumors, typically found during upper GI endoscopy performed for dyspepsia. ECLomas present frequently as multiple polyps, usually < 1 cm in diameter in the gastric fundus. Type 1 tumors are almost exclusively benign lesions with little risk of deep invasion of the gastric parietal wall. The neoplastic ECL cells become progressively dedifferentiated with an increasing number of Ki-67 immunoreactive (IR) cell nuclei. In addition, there is a substantial decrease in argynophil and IR NE cells that can be visualized by conventional methods. ECLomas secondary to hypergastrinemia should be closely followed for signs of clinical and histopathological tumor progression. Such ECLomas deserve early, active, radical surgical treatment.
Traditionally, gastric carcinoid type 1 (GCA1s) are endoscopically or surgically removed, depending on the number, appearance and size of the tumors. Antrectomy, with surgical excision of the majority of the G cells, is thought to facilitate regression of these tumors by removing the source of excessive gastrin secretion; however, the long-term benefits of antrectomy still remain uncertain. Although proton pump inhibitors are effective in reducing hypergastrinemia-induced gastric acid hypersecretion in GCA2, they do not affect ECL-cell hyperplasia, and therefore their role in GCA1 is limited. Moreover, in selected cases, significant reduction of hypergastrinemia does not prevent development of ECL carcinoid, suggesting that, in addition to hypergastrinemia, other pathogenic or genetic factors may be involved. Treatment with somatostatin analogues (SSA) might impede ECL-cell hyperplasia by suppressing gastrin secretion and/or by a direct anti-proliferative effect on ECL cells. Treatment with SSAs in GCA1 leads to a substantial tumor load reduction, with a concomitant decrease of serum gastrin levels. Published data indicate an important anti-proliferative effect of SSA on ECL cells, providing clinical benefit and obviating, at least temporarily, the need for invasive therapies for GCA1. Morphometric studies demonstrated that, while antrectomy specifically decreased the volume of ECL cells versus the total volume of endocrine cells, octreotide reduces the overall endocrine cell volume. Although the number of treated patients is small, it has been suggested that SSA may exert important anti-proliferative effects either directly, by inhibiting ECL-cells proliferation, or indirectly through suppression of gastrin hypersecretion.

Introduction: Small intestine neuroendocrine tumors (NETs) comprise well-differentiated NET (benign carcinoid), well-differentiated neuroendocrine carcinoma (malignant carcinoid) and poorly differentiated neuroendocrine carcinoma (NEC). The majority of NET patients have developed liver metastases at the time of diagnosis and surgery is then seldom curative. Novel predictive, diagnostic and prognostic markers are thus needed to improve our capabilities to diagnose and cure these tumors. We have previously identified six novel marker genes for neuroendocrine tumor cells by using Affymetrix microarrays and advanced bioinformatics. One of this markers, the paraneoplastic antigen Ma2 (PNMA2), which is normally expressed only in nervous tissue, can in the process of carcinogenesis be detected in tumors located outside the nervous system. The finding that Ma2 is expressed in small intestine neuroendocrine primary tumors and their metastases made it interesting to screen whether antibodies against Ma2 are present in the serum of NET patients.

Introduction: Gastrinomas represent a rare group of neuroendocrine tumors usually located in the duodenum or pancreas. They secrete gastrin, which is responsible for the clinical picture of severe acid-related peptic disease and diarrhea, known as the Zollinger-Ellison syndrome (ZES). While symptomatic control may be achieved with proton-pump inhibitors (PPIs) and somatostatin analogues (SSAs) treatment, little data is known regarding the possible anti-tumor effect of the peptide receptor radioligand therapy (PRRT) in gastrinoma patients.

Introduction: Although a number of familiar endocrine syndromes are associated with primary hyperparathyroidism (PHP), there is no information regarding its prevalence in other sporadic neuroendocrine diseases.

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